期刊文献+

人参皂苷Rg1对阿霉素引起的血管内皮细胞损伤的作用及机制研究 被引量:1

Ginsenoside Rg1 protects against endothelial cell injury induced by doxorubicin through antioxidation and anti-apoptosis
下载PDF
导出
摘要 目的探讨人参皂苷Rg1对阿霉素损伤后血管内皮细胞的作用及其机制。方法该研究分为正常组、阿霉素组(0.5μg/ml)、阿霉素+Rg1组(0.5μg/ml阿霉素+200μg/ml Rg1)。通过MTT法、划痕及小管形成实验检测人参皂苷Rg1对阿霉素损伤后血管内皮细胞增殖、迁移及小管形成的影响。通过Hochst33342染色和流式细胞术检测人参皂苷Rg1对阿霉素损伤后血管内皮细胞凋亡的影响。采用Western blotting检测人参皂苷Rg1对阿霉素损伤后血管内皮细胞Bcl-2、p-Akt、p-ERK及p-eNOS蛋白表达的影响。结果与正常组比较,阿霉素组细胞活性降低(P<0.05);与阿霉素组比较,阿霉素+Rg1组能提高血管内皮细胞的细胞活性(P<0.05)。与阿霉素组比较,阿霉素+Rg1组能够改善血管内皮细胞的迁移及小管形成状态(P<0.05)。与阿霉素组比较,阿霉素+Rg1组减少阿霉素引起的细胞凋亡(P<0.05)。与阿霉素组比较,阿霉素+Rg1组阿霉素损伤后血管内皮细胞NO升高(P<0.05),ROS减少(P<0.05)。阿霉素组Bcl-2、p-ERK、p-Akt及p-eNOS蛋白相对表达量较正常组低(P<0.05),阿霉素+Rg1组较阿霉素组高(P<0.05)。结论人参皂苷Rg1可减轻阿霉素引起的血管内皮细胞损伤,从而为人参皂苷Rg1治疗阿霉素引起的心脏损伤提供新的靶点。 Objective To investigate the protective effect of ginsenoside Rg1 on vascular endothelial cells injured by doxorubicin and to explore its mechanism.Methods The study consists of normal group,doxorubicin group(0.5μg/ml)and doxorubicin+Rg1 group(0.5μg/ml doxorubicin+200μg/ml Rg1).The effects of ginsenoside Rg1 on proliferation,migration and tube formation of vascular endothelial cells after injury with doxorubicin were respectively detected by MTT,scratch assay and tubule formation assay.The apoptosis of vascular endothelial cells induced by doxorubicin was detected by Hochst33342 staining and flowcytometry.The effects of ginsenoside Rg1 on the expression of Bcl-2,p-Akt,p-ERK and p-eNOS in vascular endothelial cells injured by doxorubicin were determined by immunoblotting.Results After doxorubicin injury,ginsenoside Rg1 promoted proliferation,migration and tube formation of vascular endothelial cells(P<0.05),and decreased apoptosis of vascular endothelial cells(P<0.05).Besides,compared to those of the doxorubicin group,NO was increased while ROS was reduced in the injured vascular endothelial cells of doxorubicin+Rg1 group(P<0.05).Western blot results showed that ginsenoside Rg1 increased the expression of Bcl-2,p-Akt,p-ERK and p-eNOS in vascular endothelial cells injured by doxorubicin(P<0.05).Conclusions Ginsenoside Rg1 attenuates vascular endothelial cell injury induced by doxorubicin,which provides a new target for the treatment of cardiac damage caused by doxorubicin.
作者 马铂涵 韩兵 刘婷 王一 黄建华 陶贵周 Bo-han Ma;Bing Han;Ting Liu;Yi Wang;Jian-hua Huang;Gui-zhou Tao(The First Affiliated Hospital of Jinzhou Medical University,Jinzhou,Liaoning 121000,China;Jimo Hospital of Traditional Chinese Medicine,Qingdao,Shandong 266200,China)
出处 《中国现代医学杂志》 CAS 2020年第18期1-7,共7页 China Journal of Modern Medicine
关键词 内皮 血管 细胞 心脏损伤 ginsenoside Rg1 doxorubicin vascular endothelial cells cardiac damage
  • 相关文献

参考文献1

二级参考文献16

  • 1Scully RE, l,ipshuhz SE. Anthracyeline cardiotoxieity in long-term survivors of childhood cancer [ J ]. Cardinvasc Toxicol, 2007, 7 (2) : 122-128.
  • 2Hrdina R, Gersl V, Klimtova I, et al. Anthracycline-induced car- diotoxicity [ J ]. Acta Medica ( Hradec Kralove) , 2000, 43 (3) : 75- 82.
  • 3Wang XY, Yang CT, Zheng DO, et al. Hydrogen sulfide protects H9c2 cells against doxorubiein-induced eardiotoxicity through inhibi- tion of cndoplasmic reticulum stress[ J ]. Mol Cell Biochem, 2012, 363(1-2) : 419-426.
  • 4Lou H, Danelisen 1, Singal PK. hlvcdvement of mitogen-aetivaled protein kinases in adriamycin-induced cardiomyopathy [ J ]. Am J Physiol Heart Circ Physinl, 2005, 288(4) : H1925-930.
  • 5Lou H, Kaur K, Sharma AK, et al. Adriamyein-indueed oxidative stress, activation of MAP kinases and apoptosis in isolated eardio- myocytes[ J ]. Pathophysiology, 2006, 13 (2) : 103-109.
  • 6Poizat C, Purl PL, Bai Y, et al. Phosphorylation-dependent degra- dation of p300 by doxorubicin-activated p38 mitogen-activated pro- tein kinase in cardiac cells [ J ]. Mol Cell Biol, 2005. 25:2 673-687.
  • 7Su YW, Liang C, Jin HF, et al. Hydrogen sulfide regulates cardi- ac function and tructure in adriamycin-induced cantiomyopathy [ J ]. Circ J, 2009, 73 : 741-749.
  • 8Poizat C, Purl PL, Bai Y, et al. Phosphorylation-dependent degra- dation of p300 by doxorubicin-activated p38 mitogen-activated pro- tein kinase in cardiac cells [ J ]. Mol Cell Biol, 2005. 25:2 673-687.
  • 9Wang R. Two. three crowd: 1t2S I the third compally, endog- a can nous gaseous transmitter[J]. FASEB J, 2(X)2, 16(13) : 1 792,-798.
  • 10Bian jS, Yong QC, Pan PIT, et al. Role nf hvdrogt.n sulfide in the ardioprotectinn caused by ischemic preconditioning in the rat heart and cardiac myocytes [ J ]. J Pharmacol Exp Tiler, 2006, 316 ( 2 ) : 570-678.

共引文献3

同被引文献15

引证文献1

二级引证文献3

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部